Fig. 6: The effects and mechanism of air pollution and meteorological factors on AC in Northeast China.

NO2, SO2, O3 increase allergic sensitization, induce acidification of the tears, and chemical modification of aeroallergens. High temperature and low humidity increase pollen concentration. Pollens induce IgE production and IgE attached to the IgE-FcεRI complex on mast cells (MGs), activating MGs degradation and releasing histamine. PM2.5 promotes IgE production, MGs growth, and aggregation of eosinophil cells infiltration in the conjunctiva. Allergens were presented by dendritic cells (DC), causing Th0 or CD4 cells to differentiate into Th2 cells, promoting IgE-mediated allergies by releasing IL-3, IL-4, IL-5, IL-5, IL- 9, IL-10, and IL-13, leading to eosinophilic activation and releasing histamine. Diesel Exhaust Particles (DEP) decreased the viability, proliferation, IL-8 expression and increases apoptosis, and IL-6 expression in conjunctiva epithelial cells (CEC). DEP induces conjunctiva goblet cells (CGC) hyperplasia and secrete musin to facilitate DEP clearance. DEP increases the expression of ROS, nitrogen (RNS), hydrogen peroxide (H2O2), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST). DEP decreases the expression of glutathione reductase (GR) and the total reactive antioxidant potential (TRAP) in CEC, resulting in AC